Title of article :
Cardiac Troponin After Percutaneous Coronary Intervention and 1-Year Mortality in Non–ST-Segment Elevation Acute Coronary Syndrome Using Systematic Evaluation of Biomarker Trends
Author/Authors :
Tricoci، نويسنده , , Pierluigi and Leonardi، نويسنده , , Sergio and White، نويسنده , , Jennifer and White، نويسنده , , Harvey D. and Armstrong، نويسنده , , Paul W. and Montalescot، نويسنده , , Gilles and Giugliano، نويسنده , , Robert P. and Gibson، نويسنده , , C. Michael and Van de Werf، نويسنده , , Frans and Califf، نويسنده , , Robert M. and Harrington، نويسنده , , Robert A. and Brau، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2013
Abstract :
Objectives
tudy sought to review cardiac troponin (cTn) trends during non–ST-segment elevation acute coronary syndrome (NSTE ACS) in patients undergoing percutaneous coronary intervention (PCI) in the EARLY ACS (Early Glycoprotein IIb/IIIa Inhibition in Non–ST-Segment Elevation Acute Coronary Syndromes) and SYNERGY (Superior Yield of the New Strategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors) studies and to study the relationship between post-PCI cTn and mortality.
ound
ognostic value of cTn post-PCI is controversial. In patients with NSTE ACS, it is especially difficult to distinguish between cTn elevations due to PCI or index myocardial infarction (MI).
s
nd cTn (indexed by upper limit of normal [ULN]) data pairs were plotted for 10,199 patients and independently reviewed by 2 physicians to identify patients in whom post-PCI cTn elevation could be distinguished from that of index MI. Post-PCI cTn peak was identified for each plot, and its relationship with 1-year mortality was evaluated using Cox modeling, correcting for 15 clinical variables from the EARLY ACS 1-year mortality model (including baseline cTn). We used an identical methodology to assess the association between creatine kinase-myocardial band and 1-year mortality.
s
ts with cTn (re-)elevation post-PCI not evaluable were identified and excluded from further analysis (4,198 [41%] with cTn rising prior to PCI; 229 [2%] with missing cTn). Among the remainder (n = 5,772 [57%]), in the multivariable model, peak cTn post-PCI was associated with a 7% increase in mortality (hazard ratio [HR] for 10× ULN increase: 1.07, 95% confidence interval [CI]: 1.02 to 1.11; p = 0.0038). Peak post-PCI creatine kinase-myocardial band was significantly associated with 1-year mortality (HR for 1× ULN increase: 1.13, 95% CI: 1.05 to 1.21; p = 0.0013).
sions
d a methodology that differentiated post-PCI cTn (re-)elevation from that of presenting MI in more than one-half of patients with NSTE ACS undergoing PCI. This identified a highly significant relationship between post-PCI cTn and 1-year mortality, with implications for both incorporating a cTn post-PCI MI definition and preventing PCI-related myonecrosis.
Keywords :
acute coronary syndrome(s) , mortality , myocardial infarction , percutaneous coronary intervention , Troponin
Journal title :
JACC (Journal of the American College of Cardiology)
Journal title :
JACC (Journal of the American College of Cardiology)